ArticleThe Journal of experimental medicine1998
Human immunodeficiency virus type 1 Vpr is a positive regulator of viral transcription and infectivity in primary human macrophages.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
71 citing papers in PubMed, 138 citations in OpenAlex.
- HIV-1 Vpr orchestrates ciTRAN upregulation through TGF-β induction.PLoS pathogens · 2025Article
- CRL4-DCAF1 Ubiquitin Ligase Dependent Functions of HIV Viral Protein R and Viral Protein X.Viruses · 2024Review
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- HIV-1 Vpr induces ciTRAN to prevent transcriptional repression of the provirus.Science advances · 2023Article
- Article
- Huntingtin-Interacting Protein 1 Promotes Vpr-Induced G2 Arrest and HIV-1 Infection in Macrophages.Viruses · 2021Article
- Article
- Protein ArginineViruses · 2020Article
- HIV-1 Vpr counteracts HLTF-mediated restriction of HIV-1 infection in T cells.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Proteasomal Degradation Machinery: Favorite Target of HIV-1 Proteins.Frontiers in microbiology · 2018Review
- Regulation of CD4 Receptor and HIV-1 Entry by MicroRNAs-221 and -222 during Differentiation of THP-1 Cells.Viruses · 2017Article
- HIV-1 Vpr protein directly loads helicase-like transcription factor (HLTF) onto the CRL4-DCAF1 E3 ubiquitin ligase.The Journal of biological chemistry · 2017Article
- Dual role of the chromatin-binding factor PHF13 in the pre- and post-integration phases of HIV-1 replication.Open biology · 2017Article
- HIV-1 Vpr Inhibits Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication by Inducing MicroRNA miR-942-5p and Activating NF-κB Signaling.Journal of virology · 2016Article
- HIV-1 Vpr increases Env expression by preventing Env from endoplasmic reticulum-associated protein degradation (ERAD).Virology · 2016Article
- Human Immunodeficiency Virus Infection and Host Defense in the Lungs.Seminars in respiratory and critical care medicine · 2016Review
- HIV-1 Vpr protein activates the NF-κB pathway to promote G2/M cell cycle arrest.Virologica Sinica · 2015Article
- The phosphorylation of HIV-1 Gag by atypical protein kinase C facilitates viral infectivity by promoting Vpr incorporation into virions.Retrovirology · 2014Article
- The macrophage: a therapeutic target in HIV-1 infection.Molecular and cellular therapies · 2014Review
- Efficient BST2 antagonism by Vpu is critical for early HIV-1 dissemination in humanized mice.Retrovirology · 2013Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is currently well established that HIV-1 Vpr augments viral replication in primary human macrophages. In its virion-associated form, Vpr has been suggested to aid efficient translocation of the proviral DNA into the cell nucleus. Although Vpr growth-arrests dividing T cells, the relevance of this biological activity in nondividing macrophages is unclear. Here we use Vpr-mutants to demonstrate that the molecular determinants involved in G2-arresting T cells are also involved in increasing viral transcription in macrophages, even though these cells are refractive to the diploid DNA status typical of G2 phase. Our results suggest that the two phenotypes, namely the nuclear localization and the G2-arrest activity of the protein, segregate functionally among the late and early functions of Vpr. The nuclear localization property of Vpr correlates with its ability to effectively target the proviral DNA to the cell nucleus early in the infection, whereas the G2-arrest phenotype correlates with its ability to activate viral transcription after establishment of an infection. These two functions may render Vpr's role essential and not accessory under infection conditions that closely mimic the in vivo situation, that is, primary cells being infected at low viral inputs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.